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Receptor Antagonist of IL‐13 Exerts a Potential Negative Regulation During Early Infection of Human Schistosomiasis
The pathology of schistosomiasis is associated with the formation of granulomas, and this process is associated with liver fibrosis. Studies indicate that Th1 cytokines reduce fibrosis in schistosomiasis, while Th2 cytokines play a part in the progression of fibrosis, and IL‐13 has a critical role i...
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Published in: | Scandinavian journal of immunology 2016-11, Vol.84 (5), p.284-290 |
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Main Authors: | , , , , , , |
Format: | Article |
Language: | English |
Subjects: | |
Citations: | Items that this one cites Items that cite this one |
Online Access: | Get full text |
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Summary: | The pathology of schistosomiasis is associated with the formation of granulomas, and this process is associated with liver fibrosis. Studies indicate that Th1 cytokines reduce fibrosis in schistosomiasis, while Th2 cytokines play a part in the progression of fibrosis, and IL‐13 has a critical role in this process. The IL‐13Rα2 receptor, known as a ‘receptor antagonist’ binds with high affinity to IL‐13, and studies have identified that this plays a part in reducing fibrosis and the size of granulomas. The objective of this study was to evaluate the function of IL‐13Rα2 and cellular immune response in hepatic fibrosis. A negative correlation between IL‐13Rα2 and IL‐13 was found, suggesting an increase in cytokine in early fibrosis. Initially, a negative correlation between IFN‐γ and IL‐13 was found in patients without fibrosis, and subsequently, this correlation was found to be positive in patients with severe fibrosis, thereby highlighting a new mechanism for regulating the progress of periportal fibrosis. There was a positive correlation between the profiles of Th1 and Th2 cytokines, suggesting the presence of both responses, thus regulating the disease. The results contribute to a better understanding of the immune mechanisms that control the process of hepatic fibrogenesis in schistosomiasis in humans. |
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ISSN: | 0300-9475 1365-3083 |
DOI: | 10.1111/sji.12472 |